Cardiovascular Centerhttp://hdl.handle.net/2027.42/86587
Tue, 03 Mar 2015 22:43:59 GMT2015-03-03T22:43:59ZCardiovascular Centerhttp://deepblue.lib.umich.edu:80/bitstream/id/294188/279979.gifhttp://hdl.handle.net/2027.42/86587
Exercise-Induced Hypertension After Repair of Coarctation of the Aorta: Arm Versus Leg Exercisehttp://hdl.handle.net/2027.42/86162
Exercise-Induced Hypertension After Repair of Coarctation of the Aorta: Arm Versus Leg Exercise
Markel, Howard; Rocchini, Albert P; Beekman, Robert H; Martin, Jean; Palmisano, John; Moorehead, Catherine; Rosenthal, Amnon
Tue, 01 Jul 1986 00:00:00 GMThttp://hdl.handle.net/2027.42/861621986-07-01T00:00:00ZInfluence of the MCAT on the Premedical Curriculahttp://hdl.handle.net/2027.42/85662
Influence of the MCAT on the Premedical Curricula
Markel, Howard; O'Neill, Robert; Vander, Arthur J; Noah, Terry; Zweifler, Andrew; Hornback, Bert G
Thu, 01 Apr 1982 00:00:00 GMThttp://hdl.handle.net/2027.42/856621982-04-01T00:00:00ZInduction of Human Blood Group A Antigen Expression on Mouse Cells, Using Lentiviral Gene Transductionhttp://hdl.handle.net/2027.42/85136
Induction of Human Blood Group A Antigen Expression on Mouse Cells, Using Lentiviral Gene Transduction
Fan, Xiaohu; Lang, Haili; Zhou, Xianpei; Zhang, Li; Yin, Rong; Maciejko, Jessica; Giannitsos, Vasiliki; Motyka, Bruce; Medin, Jeffrey A.; Platt, Jeffrey L.; West, Lori J.
Abstract The ABO histo-blood group system is the most important antigen system in transplantation medicine, yet no small animal model of the ABO system exists. To determine the feasibility of developing a murine model, we previously subcloned the human α-1,2-fucosyltransferase (H-transferase, EC 2.4.1.69) cDNA and the human α-1,3-N-acetylgalactosaminyltransferase (A-transferase, EC 2.4.1.40) cDNA into lentiviral vectors to study their ability to induce human histo-blood group A antigen expression on mouse cells. Herein we investigated the optimal conditions for human A and H antigen expression in murine cells. We determined that transduction of a bicistronic lentiviral vector (LvEF1-AH-trs) resulted in the expression of A antigen in a mouse endothelial cell line. We also studied the in vivo utility of this vector to induce human A antigen expression in mouse liver. After intrahepatic injection of LvEF1-AH-trs, A antigen expression was observed on hepatocytes as detected by immunohistochemistry and real-time RT-PCR. In human group A erythrocyte-sensitized mice, A antigen expression in the liver was associated with tissue damage, and deposition of antibody and complement. These results suggest that this gene transfer strategy can be used to simulate the human ABO blood group system in a murine model. This model will facilitate progress in the development of interventions for ABO-incompatible transplantation and transfusion scenarios, which are difficult to develop in clinical or large animal settings.
Fri, 01 Jan 2010 00:00:00 GMThttp://hdl.handle.net/2027.42/851362010-01-01T00:00:00ZAntiplatelet Therapy Use and the Risk of Venous Thromboembolic Events in the Raloxifene Use for the Heart (RUTH) Trialhttp://hdl.handle.net/2027.42/85099
Antiplatelet Therapy Use and the Risk of Venous Thromboembolic Events in the Raloxifene Use for the Heart (RUTH) Trial
Duvernoy, Claire S.; Yeo, Adeline A.; Wong, Mayme; Cox, David A.; Kim, Hyungjin M.
Abstract Background: Raloxifene use in postmenopausal women with osteoporosis increases the risk of venous thromboembolic events (VTE) 2-fold compared with placebo. Platelet activation is involved in the pathophysiology of arterial thromboses more than venous thromboses, but aspirin may reduce VTE risk associated with estrogen use. This analysis examines the effects of concomitant antiplatelet therapy on VTE risk in raloxifene-treated women. Methods: In the Raloxifene Use for the Heart (RUTH) trial, 10,101 postmenopausal women from 177 sites in 26 countries at increased risk of coronary heart disease (CHD) (primary prevention cohort) or with CHD (secondary prevention cohort) were randomized to placebo or raloxifene 60?mg/day and followed for a median 5.6 years. Reports of clinical symptoms of VTE were assessed. Concomitant use of antiplatelet agents (aspirin, clopidogrel, ticlopidine, dipyridamole) was allowed. Cox proportional hazard models, with use of warfarin, presence of fracture, and hospitalization as covariates, were used to estimate hazard ratios (HR) with 95% confidence intervals (CI). Results: Overall, raloxifene use was associated with an increased VTE risk (HR 1.44, 95% CI 1.06-1.95) vs. placebo. Most women (72%) reported using aspirin, and 14.2% reported using nonaspirin antiplatelet agents during the study period. Users of antiplatelet agents were older, more likely to have CHD, and more likely to be hyperlipidemic. They had a higher VTE risk than nonusers. No difference in VTE risk was observed in women who used raloxifene alone vs. those who used raloxifene with antiplatelet agents during the study. The increase in VTE risk with raloxifene compared with placebo was not different between women who used antiplatelet agents at baseline (HR 1.44, 95% CI 0.98, 2.10) and those who did not use antiplatelet agents (HR 1.37, 95% CI 0.83, 2.27) (interaction p?=?0.88). Similar conclusions were noted for aspirin and nonaspirin antiplatelet use. Conclusions: In RUTH, postmenopausal women treated with raloxifene had an increased risk of VTE compared with placebo. Concomitant use of aspirin or nonaspirin antiplatelet agents along with raloxifene did not change VTE risk.
Fri, 01 Jan 2010 00:00:00 GMThttp://hdl.handle.net/2027.42/850992010-01-01T00:00:00Z